The development of the transgenic mouse that expresses high levels of mutant APP v717-F with consequent development of diffuse and neuritic plaques is the most promising animal model of AD, and represents a breakthrough in the investigation of the inflammatory hypothesis of AD. Using this animal model it is now feasible to determine the extent and sequence of activation of inflammatory pathways by both diffuse and neuritic amyloid plaques. The proposed Pilot Project explores the role of complement system and other immuno-inflammatory molecules in brain of the amyloid precursor protein (APP)-v717-F transgenic mice bearing AD-type neuropathology and control littermates. If it can be shown that C-system activation, similar to that seen in AD is present in the brain of these mice, it will be feasible to propose future studies of anti-inflammatory interventions in the mice. These pilot studies may provide rationales, potential sites of action and timing for controlling immuno-inflammatory mechanisms in AD brain.